We have found that lactate and ascorbate enhance the accumulation of certain amino acids by the cornea of the toad, Bufo marinus. This stimulation by ascorbate and lactate is specific for neutral amino acids transported by a sodium independent system. The accumulation of leucine, a specific substrate for transport by this system is stimulated 80 percent in the presence of lactate and 30 percent by ascorbate. The addition of various inhibitors and uncouplers of mitochondrial electron transport is ineffective in blocking the increased transport caused by the addition of lactate and ascorbate. Only carbon monoxide is effective in blocking this increase in amino acid accumulation. Ascorbic acid, but not lactate, also causes a 3-fold increase in chloride transport across the amphibian cornea. This increased ion transport is not effected by cyanide or dinitrophenol. Our evidence indicates ATP is not directly involved in this response. Because ascorbate and lactate are found in rather high concentrations in the aqueous humor of most vertebrates, we feel these effects on transport are of particular interest. We have developed evidence that lactate and ascorbate are acting via an extramitochondrial electron tranport system. We propose to study this possibility in the whole tissue, in isolated cells and in cell membrane vesicles. Other investiators have reported specific effects of ascorbate on a NA ion, K ion-dependent ATPase in brain tissues. We also will study the effects of lactate and ascorbate on this enzyme.